Skepticism

EVENTS

The Lyon hypothesis, nicely illustrated

Dang, I teach all this stuff about genes and chromosomes and epigenetics, but I don’t have the advantage of giant floating holographic molecules floating around me. Maybe I’ll have to steal this for my classes.

Although it could use some discussion of Blaschko’s lines, to explain why you get a stripey pattern rather than just salt-and-pepper.

Probably the best known example is the consequences of the Dutch famine of 1944; people who survived it later produced children who were smaller than average, and most interestingly, those children grew up to produce smaller children of their own.

Why smaller children? The human body was modifying its children to cope with less nutrient – one of the triggers for sexual maturity is size and if you cant get big enough to reproduce..
One of the things that happens in plants is they seem to be able to pre-program their seeds to cope with the local environment. I’ve not been able to find any studies on this (and had an application to study it rejected) but in the the gardening world their is a lot of rumour about using your own seed rather than buying in. A lot of plants seem to produce more second or third generation even in genetically identical stock – the seed seems to hand on information its parent has worked out about which nutrients are available and how to get them so the seed gets a better start as it doesnt have to search for this itself. I’ve found it is very noticeable in some plants – 30% yield increases and better pest resistance – but I’ve not had proper mentoring (see above) so there may be some flaws…

There are also numerous studies in mice that showed that variation in folic acid in grandparents can affect grandchildren. That article was about deficiency in folic acid, but I’ve also read an article in nature (which I can’t find right now) that showed that excess folic acid caused future generations to be more obese.

Yeah. I was turning it over in my mind on the way to work today and I figured that might be it. I don’t know why but I assumed that a famine would select for hearty/fatter/more likely to retain nutrients types of bodies.

Probably the best known example is the consequences of the Dutch famine of 1944

Given the histone/methylation techniques I can see where near starvation of the embryo might cause epigenetic changes that result in a smaller adult and then pass these changes on in their germ cells even though mom was now fat and sassy (excuse me: Rubenesque and bold). Even passing into multiple generations. Environmental factors play such a strong role in development.

I was thinking of “behaviors,” though, in terms of the prototypical blacksmith’s arm, acquired attributes, the resurrection of Lamarck, not developmental environment. There is no zombie Lamarck out there seeking to dine on biologists’ brains?

Speaking of our Feline Overlords, I notice in the article on Blaschko’s lines, the graphic shows whorls on the back of the model’s leg, at the top of the thigh. On tabby cats, the Classic pattern approved by breeders has an oyster-shaped whorl just where the thigh meets the abdomen. Do the stripes develop in the same way?

PZ, one explanation I’ve heard for why women typically see colors better than men is that some of the genes for photoreceptor pigments are carried on the X chromosome. But, that would seem advantageous only if both X chromosomes are expressed in the retina. Does the striping run that finely there?Or is that explanation bogus.

rturpin, I’m pretty sure that explanation is bogus. As far as I’m aware, there is no difference in perception of colours beyond 1. Cultural effects, which expect women to be more interested in and better at colours, so they might make more distinctions even if actual colour vision is the same and 2. The fact that the genes are on the X chromosome meaning that men are more likely to be colourblind.

So, how does this interact with recessive genes on the X chromosome, like color blindness?

My understanding was always that any woman with a color blind father would be a carrier and have a 50% chance of passing on that defective copy to her children, and that if both parents passed on the defective gene in the X chromosome, the woman would be colorblind herself.

But if only one copy of the X chromosome is active, shouldn’t anyone with one defective copy have a 50% chance of being colorblind? In each eye, even?

@Nick Johnson #19: Both X chromosomes are active in any given person; it’s only at the level of individual cells that it’s one or the other. You do get the “stripe” effect, but that’s below the level of a whole organ like an eye. At least that’s what I got from the video. :)

The narrator of this piece says something like, “of course, one of the two copies of the X chromosome has to be silenced.” But why? We have two of all the other chromosomes, and I’ve always understood that both copies were active. Why is the X chromosome different?

So, if a) one of a woman’s X chromosomes is deactivated, b) at random, and c) all retinal cells are from the same cell, then women should have the same probability of color blindness as men. If they gain advantage from that second X chromosome, either genes from both are being expressed where that matters. Or the X chromosome with better color vision genes is preferentially made the active chromosome. That last seems quite unlikely.

I share some of the confusion. It’s upending my understanding of how genes and chromosomes work. I always thought that dominance and recessiveness happened at the gene level, not the chromosome. Now it makes no sense at all. How can genes be dominant to recessive if the whole chromosome is deactivated at random.

For instance I was taught at one point that the brown eye gene dominates over the blue eye one, so if you have one of each gene you’ll have brown eyes. Does this striping account for people and critters with one brown and one blue?

Also, does this only apply to XX pairs, or to all other pairs?

What about haemophilia? My understanding is that women can carry it, but it’s recessive. Do women half their cells with it active and half not, so maybe they have half the amount of clotting agent in their blood as normal folks?

All mammals are XY. ZW is birds (and some crustaceans, and some fish, and some insects, and some reptiles, so I guess it’s paraphyletic).

That, or its just humans choosing to name monophyletic chromosomes differently. Perhaps so that the mammals can stand out from the crowd, because humans are mammals and humans do so like to feel special.

AFAIK, only one photoreceptor gene is on the X chromosome, and that’s the one that causes red-green colour-blindness.

The fact that this is much more common in men does strongly suggest that the retinal photoreceptor cells in females have a mixture of the 2 X’s activated.

There is a, I think, controversial, claim that some women are tetrachromats. They have a mutant version of the red-green photoreceptor on one of their X’s that is active but with a shifted spectrum of sensitivity, giving them 4 total. Not that different from how some of the New World monkeys manage trichromatic colour vision (which only the females have).

But assuming there is no mutant alleles, there is no genetic reason for women to have better color vision than men (who are not red-green color blind). IF such a difference actually exists, then the cause has to be environmental. If girls are taught from a young age that distinguishing colors is important, and given lots and lots of opportunities to practice at it in daily activities they are encouraged to do, then it would stand to reason that their brains become better at it, seeing as the majority of color processing actually occurs in the brain.

Seeing that only one X chromosome is needed what is left on the Y that tells the cells this human is going to be a man?

Different genes giving different proteins resulting in different structures.

not…much…information there.
Most mammalian cells don’t “know” their chromosomal sex; they don’t have to. There are a few genes on the Y ‘some, one of which, SRY, flicks the genetic switch that induces the undifferentiated fetal gonads to become testes. Testes secrete testosterone, and it’s via the hormonal signal that all other cells that are sexually difunctional get the sex message.

one explanation I’ve heard for why women typically see colors better than men

[citation needed]
There is afaik some limited evidence that some women can differentiate among colors more finely than other humans of any gender, but the idea is that there can be different alleles for the photopigment genes on the X chromosome, such that they have slightly diferent color/wavelength-absorption properties, and because genes on both X homologs are expressed in the retina (see below), they can be using more different pigments. [link]. Not clear to me how the brain’s visuial cortex is able to integrate 4 (or more?) inputs instead of the usual 3, but…

My understanding was always that any woman with a color blind father would be a carrier and have a 50% chance of passing on that defective copy to her children, and that if both parents passed on the defective gene in the X chromosome, the woman would be colorblind herself.

true

But if only one copy of the X chromosome is active, shouldn’t anyone with one defective copy have a 50% chance of being colorblind? In each eye, even?

But X-chromosome-inactivation occurs at a smaller scale, such that there are patches of photoreceptors within each retina expressing different X-linked genes. Apparently brains can integrate the patches and fill in the missing information during the perception stage. But with small enough light inputs (e.g. lasers), the retinal patches can be mapped. (It’s called ‘mosaic’ gene expression; another example iirc is patches of skin with disfunctional sweat glands because of an X-linked loss-of-ion-channel-function mutation.)

one of the two copies of the X chromosome has to be silenced.” But why? We have two of all the other chromosomes, and I’ve always understood that both copies were active. Why is the X chromosome different?

It has to do with gene dosage. All of the genes (without redundant analogs elsewhere) on the X chromosome have to be able to function with only one copy of each gene, because half of the species has only one. So cellular processes are calibrated to a one-copy dose for X-linked proteins, instead of the usual 2-gene dosage. Gene dosages can (but don;t always) have major effects, as illustrated by the obvious effects of trisomy 21 and the fact that all other trisomies and monosomies are pretty much fatal.

if a) one of a woman’s X chromosomes is deactivated, b) at random, and c) all retinal cells are from the same cell, then women should have the same probability of color blindness as men.

true, but as mentioned, c is incorrect (that is, retinas are derived from many cells that underwent X-deactivation independently).

also, does this only apply to XX pairs, or to all other pairs?

Only X chromosomes are inactivated. For the most part, genes on all autosomes are expressed in a 2-gene dosage.

What about haemophilia? My understanding is that women can carry it, but it’s recessive. Do women half their cells with it active and half not, so maybe they have half the amount of clotting agent in their blood as normal folks?

Yes, heterozygous women have less Clotting Factor VII than others, but it’s sufficient for acceptable clotting to occur.

Does the environmental conditions that the eggs and sperm are in when people are in famine situations for example change? Do the ones with the ‘taller’ codes not fare so well? I’m just wondering what the mechanism is? (And no alas, I’m one of those physicists, but at least one that is willing to admit that she knows very little about biology, but still more than most of the GOP)